The aims of this study: 1)Determine if fat raising NEFA's in lean normotensives reproduce hemodynamic abnormalitites observed in obese hypertensives including elevated BP, enhanced vascular tone and neurovascular reactivity, and impaired endothelium-dependent vasodilation. 2)Determine if lowering NEFAs in obese hypertensives decrease BP, reduce vascular tones and neurovascular reactivity, and enhance endothelium- dependent vasodilation. 3)Determine the signal transduction mechanism(s) by which NEFAs induce mitogenesis and enhance proliferative effects of angiotensin in vascular smooth muscle cells. 4)Identify the PKC-in dependent mechanism(s) by which these same NEFAs impair NOS activity in endothelial cells and endothelium-dependent vasodilation in vascular tissue